Glutathione, a tripeptide molecule, occurs naturally in mammalian cells and is an important antioxidant. The reduced form of glutathione, GSH, readily donates a reducing equivalent to unstable molecules, and is thus vital to combating oxidative stress in cells and the cell death that is a consequence of such stress. Upon donation of a reducing equivalent, GSH becomes reactive and binds with another reactive GSH to form glutathione disulfide (GSSG), which is then converted to GSH by the enzyme glutathione reductase.
Healthy cells generally maintain a 9:1 GSH to GSSG ratio. A decrease in the ratio of GSH to GSSH is indicative of oxidative stress. Oxidative stress may result in cell death and is involved in the pathophysiologic processes of many diseases, including pancreatitis.
Pancreatitis is an inflammatory condition of the pancreas that is painful and may be fatal. The mortality rate for acute pancreatitis has remained at about 10% despite medical advances, while the mortality rate for chronic pancreatitis is estimated at 70-80% within 10 years of diagnosis. It is known that GSH depletion as a result of xenobiotic or oxidative stress plays a significant role in the development of pancreatitis.
Previous methods of treating pancreatitis using glutathione precursors have been unsuccessful and, in some cases, detrimental to patients. For example, one study, found at http://gut.bmj.com/cgi/content/full/56/10/1439, which is hereby incorporated by reference in its entirety, found no therapeutic response when treating subjects with glutathione precursors and, in fact, found a slightly worse outcome in their conditions.